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Biomedical subjects

P S Gibbs

Publications and source records attributed to P S Gibbs.

At least 19 recordsLinked to original sources
PubMed1994

Antimicrobial effect of combinations of EDTA-Tris and amikacin or neomycin on the microorganisms associated with otitis externa in dogs.

Combinations of EDTA-Tris and two aminoglycoside antibiotics (amikacin and neomycin) were tested for synergistic activities against the microorganisms associated with otitis externa in dogs and for the solutions' stability over time. Synergistic activity was observed when EDTA-Tris plus amikacin and EDTA-Tris plus neomycin were tested against Staphylococcus intermedius, Proteus mirabilis, Pseudomonas aeruginosa, and Escherichia coli, but not against Candida albicans. Stability studies over a 3-month period indicated that the test solutions were stable at room temperature and that their antimicrobial activity was maintained.

Amikacin↗
PubMed1991

Activation of thymocyte deoxyribonucleic acid degradation by endogenous glucocorticoids.

Immature lymphocytes in the thymus gland are killed by treatment with exogenous glucocorticoids. This steroid-mediated lymphocytolysis is preceded by numerous alterations in lymphocyte metabolism, including a DNA-degrading process in which the genome is cleaved at internucleosomal intervals. To date, this process has only been characterized by treating lymphocytes in vitro with glucocorticoids or by exogenous treatment of whole animals with adrenal steroids. To determine whether thymocyte DNA degradation could be activated by endogenous glucocorticoids, 4-wk-old chicks were treated with porcine adrenocorticotropic hormone (ACTH). This procedure elevated serum corticosterone levels approximately 80-fold within 2 h of hormone treatment. Following ACTH administration, thymocyte DNA was isolated and analyzed by agarose gel electrophoresis. The ACTH activated a DNA-degrading process that generated internucleosomal fragments of DNA identical in size to those observed following exogenous treatment with synthetic or naturally occurring glucocorticoids. Furthermore, this response could be inhibited by the glucocorticoid antagonist RU486 (17 beta-hydroxy-11 beta, 4-dimethylaminophenyl-17 alpha-propynl-estra-4,9,diene-3-one), indicating that adrenal steroids activate this process via the glucocorticoid receptor. These results demonstrate that lymphocyte DNA degradation does not result solely from exogenous glucocorticoid treatment; moreover, endogenous glucocorticoids can mediate this process and may thereby play an important role in thymic gland function.

Adrenocorticotropic Hormone↗
PubMed1990

Glucocorticoid-mediated activation of DNA degradation in avian lymphocytes.

Little information is known about the molecular mechanism of programmed cell death in the avian species. In the current study we have analyzed this process in chickens using a glucocorticoid-lymphocyte model system. Three-week-old male broiler chicks were treated in vivo with the synthetic glucocorticoid, dexamethasone. Following this treatment genomic DNA was isolated from thymocytes and analyzed by agarose gel electrophoresis. Dexamethasone activated a DNA degrading process in which the genome was specifically cleaved at internucleosomal intervals. This steroid-induced response occurred prior to thymocyte cell death and was time and glucocorticoid dose dependent, as well as tissue and steroid specific. Only the glucocorticoid class of steroid hormones could elicit this response and DNA degradation was only detectable in lymphoid tissues that contained immature lymphocytes. Internucleosomal DNA degradation could also be elicited via administration of adrenocorticotrophic hormone, a treatment that elevates endogenous glucocorticoids. Based on these data, glucocorticoid-activated DNA degradation of the avian thymocyte genome appears to be a steroid receptor-mediated process which involves the activation of an endogenous nuclease that cleaves the genome at internucleosomal sites. Degradation of the thymocyte genome occurs prior to cell death and may represent an initial event in a cascade of hormone-mediated processes that culminate in a type of cellular suicide referred to as programmed cell death.

Animals↗
PubMed1990

Glucocorticoid activation of deoxyribonucleic acid degradation in bursal lymphocytes.

Treatment of animals with exogenous adrenal steroids or elevation of endogenous glucocorticoids results in a profound involution of lymphoid tissue. In rodent species, this lymphoinvolution is accompanied by lymphocyte cell death and extensive degradation of the genome prior to lymphocytolysis. In the present study, this process was investigated in the bursa of Fabricius of domestic fowl. Four-wk-old chicks were treated with a single injection of dexamethasone, and bursal regression and cell viability were monitored over a 72-h period. Following hormone treatment, DNA was extracted from bursal lymphocytes and analyzed by agarose gel electrophoresis. Dexamethasone treatment resulted in a rapid regression of bursal tissue that could be detected as soon as 6 h posttreatment, but lymphocyte viability was not altered until 24 h afterward. The DNA isolated from bursal lymphocytes of glucocorticoid-treated birds appeared to be degraded at internucleosomal sites and generated a "ladder" of discrete DNA fragments when analyzed by agarose gel electrophoresis. This form of hormone-induced cell death, referred to as programmed cell death, may play a key role in glucocorticoid-mediated immunosuppression.

Animals↗
PubMed1983

Transient paralysis of the diaphragm following radical neck surgery.

We have observed transient diaphragmatic paralysis with high alveolar to arterial oxygen partial pressure difference following radical neck surgery. Patients required supplemental oxygen for maintenance of arterial oxygenation. Patients following radical and neck surgery should be followed with chest roentgenograph to exclude pneumothorax and diaphragmatic paralysis and arterial blood gases in the immediate postoperative period.

Aged↗
PubMed1982

Evidence for acute cellular changes in human hepatocytes during anesthesia with halogenated agents: an electron microscopic study.

Liver biopsy specimens of 24 patients who had elective laparotomies were studied by electron microscopy for evidence of anesthesia-related toxic changes. All patients were initially anesthetized with nitrous oxide, barbiturate, and narcotic until the laparotomy incision was completed and an initial preanesthesia liver biopsy specimen was taken. Patients were then give, in randomized fashion, maintenance inhalational anesthesia for the duration of the procedure with halothane, fluroxene, or enflurane. Control patients were continued on nitrous oxide, barbiturate, and narcotic. After approximately 60 minutes a second postanesthesia liver biopsy specimen was taken. For each patient, the preanethesia and postanesthesia liver biopsy specimens were compared, in blinded fashion, for evidence of morphologic changes resulting from anesthesia. Ultrastructural changes consistent with hepatic toxicity were present in more than 25% of the cells examined in the postanesthesia specimens in all of the seven patients given halothane, five of the six patients given fluroxene, and one of the five patients given enflurane. None of the six nitrous oxide-barbiturate-narcotic control patients showed toxic changes in postanesthesia specimens. The most prominent toxic change was dilatation of endoplasmic reticulum. Accumulation of intracellular inclusions occurred in some cells, and a small percentage of cells also showed lipid accumulation and mitochondrial swelling. Evidence suggested that exposure to halogenated anesthetics is related to acute toxic subcellular changes in hepatocytes.

Adolescent↗
PubMed1981

Sodium intake alters the effects of norepinephrine on the renin system and the kidney.

To examine the interactions between sodium intake and the sympathetic nervous system and their influences on the blood pressure control system we studied eight normotensive men after high (800 mEq/d) and low (10 mEq/d) sodium intake. We measured blood pressure, arterial, venous and urinary norepinephrine (NE), glomerular filtration rate (GFR), renal blood flow (RBF), plasma renin activity (PRA) and aldosterone (PA), and the fractional excretion of sodium (FENa) and potassium (FEK) before and during incremental infusion of norepinephrine. High salt intake influenced the sensitivity to NE as well as subsequent pressor responses. The NE-induced decrease in RBF and GFR was not different on high and low sodium intakes. A significant decrease in FENa (p less than 0.05) with NE infusion could only be seen during high sodium intake. A significant increase in PRA (p less than 0.01) and PA (p less than 0.05) was induced by NE only during the low sodium period. These observations reveal previously unrecognized qualitative and quantitative interactions between sodium homeostasis and norepinephrine which are capable of influencing blood pressure in man.

Adult↗
PubMed1980

Reduction of enflurane-induced spike activity by scopolamine.

The possibility of enflurane-induced spike activity being related to a cholinergic mechanism was investigated. Thirty mongrel dogs were anesthetized with an inspired enflurane concentration of 3.5 +/- 0.09% (mean +/- SD) to obtain a sustained EEG spike activity. Scopolamine, in 0.04 mg/kg to 0.4 mg/kg IV doses, significantly decreased the spike activity (p less than 0.05). We speculate that a central cholinergic muscarinic mechanism is at least partly responsible for the EEG spike activity produced by enflurane.

Action Potentials↗
PubMed1979

Significance and application of blood gas determinations from the left atrial catheter.

Left atrial catheters are used to measure left heart filling pressure in patients after open-heart surgery. It was observed that in some patients blood gases obtained from the left atrial catheters had a markedly higher PO2 as compared to PaO2 in the presence of severe hypoxemia. Twenty-five patients were studied consecutively; pulmonary venous admixture calculated from arterial blood was higher in 19 patients and lower in 5 as compared with that calculated from blood withdrawn from the left atrial catheter. These differences in venous admixture are due to regional changes in the lungs. This observation can be utilized in concentrating respiratory therapy to the regions of the lungs involved with significant therapeutic benefit to the patient.

Adult↗
PubMed1979

Vascular compartmentalization of plasma norepinephrine in normal man: the relationships between venous and arterial norepinephrine concentration and the urinary excretion of norepinephrine.

To examine whether the concentration of NE in human plasma is dependent on the vascular source of the sample and to examine the contribution of the kidney to urinary NE, 14 normal men were studied. Plasma samples were obtained from a superficial forearm vein, and radial artery and urine samples were obtained during 1 hr of recumbency and 1 hr of upright posture. The Vne was greater than Ane during both recumbency and upright posture in black males. Such differences were not seen in age-matched white subjects. Stimulation of the sympathetic nervous system by upright posture increased both Vne and Ane in all subjects. NE concentrations in simultaneously obtained arterial and venous samples were different during the time of cardiovascular adjustments to upright posture. The urinary Xne increased after standing. Endogenous CCr decreased, whereas apparent NE clearance, calculated from the Ane, increased after standing, suggesting that a major portion of the augmented urinary Xne induced by upright posture was from an intrarenal source. We conclude that the concentration of NE in human blood is related to the specific vascular bed from which the sample is obtained, and that urinary NE is not solely derived from plasma by glomerular filtration but also arises from an unidentified renal source.

Adult↗
PubMed1976

Hypocalcaemia during rapid blood transfusion in anaesthetized man.

In anaesthetized patients, administration of citrated whole blood for 5 min at controlled rates of 50, 100 and 150 ml/70 kg/min resulted in decreases in the calcium ion concentration (Ca2+) of 14, 31 and 41%, respectively. Ca2+ returned rapidly to the control values after termination of the transfusion. Reciprocal changes in serum citrate concentrations occurred, suggesting that the transient hypocalcaemia was a result of redistribution of citrate and hepatic or renal clearance from the vascular space. The total serum calcium concentration did not change significantly during rapid blood administration. Normal saline infusion at 100 ml/70 kg/min caused no change in Ca2+; however, plasma protein administration at this rate resulted in an 18% decrease in Ca2+, presumably as a consequence of the binding of calcium ions to anionic sites on plasma protein. Hypocalcaemia accompanying blood transfusion is a transient phenomenon, dependent on the total dose of citrate administered and the rate of infusion. Rational calcium replacement therapy during massive blood transfusion may now be based on direct Ca+ measurement.

Anesthesia↗
PubMed1975

Hemodynamic and ventilatory responses to fentanyl, fentanyl-droperidol, and nitrous oxide in patients with acquired valvular heart disease.

Fentanyl (10 mug/kh) or fentanyl (10 mug/kg) plus droperidol (100 mug/kg) administered intravenously during 20 minutes to adult patients with acquired valvular heart disease produced minimal circulatory changes. The trend during drug infusion was for mean arterial pressure and systemic vascular resistance to decrease, and for cardiac index and stroke volume index to increase without change in heart rate. Central venous pressure increased during drug infusion (P less than 0.05) but decreased to awake levels following controlled ventilation and skeletal-muscle paralysis, probably reflecting thoracoabdominal-muscle rigidity rather than a circulatory response. Hypoventilation during drug infusion necessitated assisted or controlled ventilation, with or without skeletal muscle paralysis, in 14 of 16 patients. Addition of 60 per cent nitrous oxide following fentanyl or fentanyl-droperidol infusion significantly decreased mean arterial pressure, heart rate, and cardiac index. All circulatory changes were similar in direction and extent to those previously found during morphine-nitrous oxide anesthesia. (Key words: Anesthetics, intravenous, fentanyl; Anesthetics, gases, nitrous oxide; Heart, effect of fentanyl, dorperidol, and nitrous oxide.).

Adult↗